The concepts of heredity and degeneration in the work ofJean-Martin CharcotOlivier Walusinski

Independent Researcher, Brou, France

ABSTRACTTranscripts of the Tuesday Lessons at La Salpêtrière Hospital show thatJean-Martin Charcot often asked his patients about their family history.The information gathered on patients’ heredity played also a significantrole in the diagnostic reasoning he instructed his students in. Again andagain, he included in his teachings the concept of degeneration tosuggest an etiology for observed pathologies. This article analyzes theorigin of Charcot’s knowledge, imparted in the Tuesday Lessons, byexamining the theories of heredity and degeneration successivelydeveloped by Prosper Lucas (1808–1885) in 1847, Bénédict-AugusteMorel (1809–1873) in 1857, and Jacques-Joseph Moreau de Tours (-1804–1884) in 1859. I will review examples taken from the TuesdayLessons to illustrate how Charcot assimilated the ideas of these alienists.Two of his students, Charles Féré (1852–1907) and Georges Gilles de laTourette (1857–1904), known for championing their master’s work,went on to publish their own books that developed theories of heredityand degeneration. I will conclude my review, which aims to examine alittle known facet of Charcot’s work, with a few examples from theseauthors’ writings.

KEYWORDSCharcot; Morel; Lucas;Moreau de Tours; Féré; Gillesde la Tourette; heredity;degeneration theory; LaSalpêtrière; history ofneurology

What we know is the major obstacle to acquiring knowledge of what we don’t know.Claude Bernard (Bernard 1865)

By the middle of the nineteenth century, the anatomoclinical method developed by RenéLaennec (1781–1826) was fully deployed by Jean-Martin Charcot (1825–1893; see Figure 1).This experimentalmethod, and that introduced by Claude Bernard (1813–1878), freedmedicine—and research on nervous system diseases, in particular—from doctrinal systems it hadconveyed, in a fog of speculative philosophies, for centuries. One of the pillars of medicalreasoning remained particularly fragile: the concept of heredity. Influenced by the lectures ofAuguste Comte (1798–1857) on positive philosophy, Charcot set himself the task of establishinglaws governing the pathologies he encountered, through logic and observation, in line withexperiments involving anatomical dissections and observations compiled by Giovanni BattistaMorgagni (1682–1771) during the eighteenth century (Lellouche 1992; Morgagni 1761). He wasan adept of this scientific medicine, as he described it in the introduction to his Clinical Lectureson Diseases of Old Age (the original French was published in 1867). His collaboration withClaude Bernard (1813–1878) in his early years bears witness to this scientific mindset (Bernardand Charcot 1851).Whereas Claude Bernard favored physiology over anatomy, Charcot’s credo

CONTACT Olivier Walusinski walusinski@baillement.com Independent Researcher, 20 Rue de Chartres, Brou28160, France

JOURNAL OF THE HISTORY OF THE NEUROSCIENCEShttps://doi.org/10.1080/0964704X.2020.1717230

© 2020 Taylor & Francis

was the “supreme jurisdiction of the clinical” over anatomy and physiology. Yet, apparentlywithout realizing it, he remained, in fact, a prisoner of empirical medicine, adhering to theconcepts of degeneration and hereditary transmission of nervous system diseases (Charcot1867). As established by Goetz, Bonduelle, and Gelfand (1995), “Far from Bernardian vivisec-tional experiments, Charcot’s clinical gaze hearkened back to the great naturalist Cuvier’snoninterventionist observation of nature’s experiment (Georges Cuvier 1769–1832) and beyondthat to the first generation of Paris clinicians who sought to follow the precedent of the surgeon’spenetrating but essential observational epistemology” (55). After reviewing the state of

Figure 1. Unpublished photo of Jean-Martin Charcot by Albert Londe (1858–1917) (OW collection).

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knowledge available to Charcot in these domains, I will bring it to bear on his descriptions ofa few neurological diseases to better grasp this facet of his work.

Since time immemorial, we have been aware of the transmission of physical characteristicsfrom parents to their children, and have tried to understand how this happens. Michel deMontaigne (1533–1592) expressed his own interrogations on this subject in 1582: “What isthis monster carried within this drop of seed from which we are produced—the impressionsnot only of bodily form, but also the thoughts and inclinations of our fathers?Where does thisdrop of water house this infinite number of forms?”

Gregor Mendel (1822–1884), recognized as the founder of genetics, was Charcot’scontemporary, and his experiments on peas date from 1857, the year Charcot failed hisfirst agrégation exam (to enter the path to professorship). Yet Charcot was certainly unawareof the publication (Mendel 1865) on what would later be named the laws of Mendel(Genopole 2020). So what knowledge was at his disposal? In the mid-nineteenth centuryin France, three authors had proposed theories of heredity: Prosper Lucas (1808–1885) in1847, Bénédict-Auguste Morel (1809–1873) in 1857, and Jacques-Joseph Moreau de Tours(1804–1884) in 1859.

At this time, heredity was considered a legal and institutional concept that governed thetransmission of titles and property within families. Certain political events, such as theabolition of the transmission of certain legislative titles (hérédité de la pairie) in 1831, andthe end ofmajorat arrangements (attribution of most of the patrimony to the eldest male heirin the family) in 1835, may have influenced the thinking of Lucas and Morel. Conservativesand the clergy saw these new developments as destabilizing successional regimes andthreatening social continuity between generations; at the same time, alienists were bringingthe contingencies and risks of heredity to light. After a law pertaining to the insane was votedon under King Louis-Philippe I in 1838, the medicalization of heredity extended the medicalscope to the organization of social life, which was split between counterrevolutionaryCatholic traditions and the emergence of a social Catholicism aimed at improving the fateof the poorest citizens (Dowbiggin 1991; Hochmann 2018). As the same time, we cannotminimize the desire of alienists to acquire specific knowledge with which to advise families,and which would have enhanced their standing as well as distinguished them from themultitude of healers competing with them for the treatment of mental illness.

Georges-Louis Leclerc, Count of Buffon

Georges-Louis Leclerc, Count of Buffon (1707–1788) and director of the Royal Garden ofMedicinal Plants, was the first author to use the term “degeneration” in his treatise on thevariability of human appearance (de Buffon 1749). For him, all men were originally white,but the skin color of some of their descendants changed due to environmental influences,which he interpreted as degeneration.

Prosper Lucas and his Traité philosophique et physiologique de l’héréditénaturelle

Prosper Lucas, born on November 4, 1808, into a wealthy and influential family in Saint-Brieuc (Brittany), went to Paris to study medicine (no portrait of Lucas exists). Hedefended a remarkable thesis on August 28, 1833, before a jury presided over by

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Gabriel Andral (1797–1876). Entitled De l’imitation contagieuse ou de la propagationsympathique des névroses et des monomanies (On contagious imitation or sympatheticpropagation of neurosis and monomania; Lucas 1833), it was inspired by Franz-JosephGall (1758–1828) and Pierre Jean Georges Cabanis (1757–1808) and could serve asa historical introduction to the discovery of mirror neurons in our brains as well asa study of mass psychology (Figure 2). Lucas was first absorbed by political life, the 1848Revolution, and his own failures to convince the electorate. His career as an alienist onlystarted in 1864, when he took over at the Bicêtre asylum from Louis-Victor Marcé(1826–1864), who had recently committed suicide (Luauté and Lempérière 2012). His

Figure 2. Thesis of Prosper Lucas in 1833 (OW collection).

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first resident was Valentin Magnan (1835–1916). On March 31, 1867, Lucas began hisposition as chief physician of the recently inaugurated Women’s Division of the Cliniquede Sainte-Anne asylum, recently inaugurated. With Magnan, Gustave Bouchereau (1835–-1900), and Henri Dagonet (1823–1902), he initiated clinical lectures on mental pathologyat this asylum in 1872, acting as dean. The next year, his lessons were interrupted by thePrefect of the Seine following a press campaign orchestrated by the newspaper Le Figaro.Critics objected to his exhibition of insane patients during his lectures. Although thecontent of his teachings was not published, the title in the notices for his classes is explicit:“The importance of the science of mental illness and why its study is necessary forphysicians and judges, from various viewpoints in modern society.” Retiring in 1879,Lucas left Paris for his property in Mennecy, south of Corbeil-Essonnes (50 kilometerssouth of Paris), where he died on April 2, 1885 (Trehiou 1993).

The publication of his voluminous Traité philosophique et physiologique de l’héréditénaturelle dans les états de santé et de maladie du système nerveux (Philosophical andphysiological treatise on natural heredity in states of health and nervous system disease),over 1500 pages published in two volumes in 1847 and 1850, not only ensured him lastingfame but also inspired Charles Darwin (1809–1882) and Émile Zola (1840–1902). Darwinread Lucas’s treatise in 1856, as he indicated in his notes, published in 1987 (Barrett 1987),and used several of Lucas’s examples to support his theory, presented in 1868 in TheVariation of Animals and Plants under Domestication (Darwin 1868), and in 1871 in TheDescent of Man, and Selection in Relation to Sex (Darwin 1871). What Zola took from thistreatise were his deterministic ideas about the human species, which he put into play withthe Rougon-Macquart family (Hamon 1983). As for César Lombroso (1836–1909) andThéodule Ribot (1839–1916), they took from this treatise the concept of morbid heredity.

Lucas started by mentioning his predecessors, such Antoine Louis (1723–1792; Louis1749) and notably the 1828 hybridization experiments of Charles Girou de Buzareingues(1773–1856), a forerunner of Mendel working in the Rouergue region of southern France(Girou de Buzareingues 1828). Lucas’s book, which smacks of scholasticism but reveals hisvast erudition, is dense, full of digressions, and hard to read. In summary, Lucas sawprocreation as obeying two laws, “innateness, or the law of expression of the diverse, andheredity, or the law of expression of the similar.” Innateness, or “law of invention,” is“what constitutes the originality, imagination, and liberty of life in mediate generation,”which can be understood in terms of trait variability and phenotype. Lucas used thequalifier of invention, which is similar to adaptation in Darwin and would become theidea of mutation. Heredity, or “law of imitation,” represents “what constitutes the repeti-tion and memory of life in the same type of generation,” which he understood asgenotype. Lucas saw heredity as “the immutability of the nature of species,” the basisfor the fixism in which he believed. In the many examples he cited, he confused geneticallydetermined traits (albinism, for example) and embryogenic defects (harelip, for example).Lucas refuted numerous legends, such as “the action of imagination on coitus” and therole of adultery in malformations, attributed at that time to heredity (Figure 3).

He also added the idea of heredity of similarity and heredity of metamorphosis; in thefirst case, a disease was transmitted identically, whereas in the second, a nervous diseaseemerged in the descendant, differentiating him or her from the ascendant. Heredity maybe a predisposition, “heredity of the seed”—that is, a latent state that may or may not berevealed at a given time in life, or be a potential and variable disease state. For Lucas, this

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theory manifested itself during mental illness and was mixed together with notions of“return heredity” (or atavism, by which one resembles ancestors rather than parents),heredity of influence (influence of places and climate), and homochronic heredity (corre-spondence of age of manifestation; see Table 1). His theory attempted to explain situations

Figure 3. Cover of Volume 1 of the work by Prosper Lucas (OW collection).

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that are no longer considered to relate to genetic transmission: goiter, impulses, passions,propensity for crime, and so forth. In this way, heredity was akin to sociological explana-tions: “The study and the most infallible expression of what is organic, morbid, and fatalin human nature” (Lucas 1833). This opened the way to medical–legal and anthropolo-gical studies of criminality, at the end of the century, by César Lombroso in Italy andAlphonse Bertillon (1853–1914) in France.

Lucas applied these concepts of innateness, heredity of similarity, and heredity ofmetamorphosis to many pathologies, including convulsions, apoplexy, dementia, chorea,mental illness, hysteria, and hypochondria. And also Charcot referred to Lucas’ workmultiple times in his publications. In contrast, Louis Pasteur (1822–1895) and his studentsdestroyed Lucas’s demonstrations of hereditary transmission for diseases such as tetanus,syphilis, meningitis, and tuberculosis. In any case, Lucas’s treatise had considerableinfluence on alienists and on the work of Morel, in particular.

Bénédict-Augustin Morel and his Traité des dégénérescence physiques,intellectuelles et morales

Bénédict-Augustin Morel was born on November 22, 1809, in Vienna during the NapoleonicWars (Figure 4). His father was an army supplier and followed the troops; no informationabout his mother is available. In 1814, he was sent to a boarding school in Luxembourg. As anadolescent, he was expelled from the seminary, where his tutor had arranged his enrollment,after students rioted in favor of liberal ideas. Morel then moved to Paris and started medicalstudies while working as a tutor in a rich family. He shared the hardships and poverty studentsfaced at the time with Claude Bernard, who had come to the capital from Lyon. They becameclose and lasting friends. He defended his thesis on August 6, 1839, before a jury presided overby Jean-Nicolas Marjolin (1780–1850): Questions sur les diverses branches dessciences médicales (Questions on the various branches of the medical sciences; Morel 1839).The second question dealt with delirium. He doubted that it was localized in the cortical areaof the hemisphere, as his anatomical observations had revealed no lesions. He distinguishedbetween acute delirium, “sympathetic in origin”—that is, linked to a transient general cause,such as fever or alcohol—and the chronic delirium of the insane. Claude Bernard, thena resident at La Salpêtrière, introduced him to Jean-Pierre Falret (1794–1870), who broughthim to his department for the insane and helped him enter the French Medical-PsychologicalSociety. As encouraged by Falret, he attempted to show that alienists erred by neglecting the

Table 1. Some definitions of terms used in this article.Term Definition

Heredity of similarity or immediateheredity

A disease is transmitted identically.

Heredity of metamorphosis orheredity of transformation

A nervous disease emerges in the descendant, differentiating him or her fromthe ascendant.

Heredity of predisposition ordissimilar heredity

A latent state that may or may not be revealed at a given time in life, or bea potential and variable disease state.

“Return heredity” or atavism Resemblance with ancestors rather than parents (transmission of characteristicsjumping one or more generations, with possibly a backward jump; origin of theterm “returning heredity”).

Heredity of influence Influence of place and climate.Homochronic heredity Correspondence of age of manifestation.

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psychological aspect of insanity, instead giving priority to anatomopathological research.Antoine Ritti (1844–1920) reported that the student comradery with Claude Bernard alsoextended to Charles Lasègue (1816–1883; Ritti 1885). Lasègue took advantage of Morel’sfluency inGerman for his historical research on the doctrines of Stahl andGerman psychology(Lasègue and Morel 1844), research that would lead to Lasègue’s (1846) thesis, defendedbefore a jury presided over by Armand Trousseau (1801–1867) on February 25, 1846 (Falret1873).

After the 1848 Revolution, Morel was named chief physician of the Mareville asylumnear Nancy, in northern France. An adept of nonrestraint, he did away with chains andother brutal measures as well as prison-like cells. Starting in 1851, he began clinicallectures on mental illness. The premises of his thinking on degeneration were laid withhis observations of patients suffering from goiter and of cretins at the Rosières auxSalines center, near Nancy, whom he also treated. On May 23, 1856, Morel was named tothe Saint-Yon asylum near Rouen, “where he remained the chief physician until hisdeath. There he would develop and complete the studies and works he began in Nancy,and start work on his volume on degeneration in the human species, published in 1857,which was the most significant and important work of his life,” according to Jules Falret(1824–1902), speaking at his funeral (Falret 1873). Weakened over several years bydiabetes, Morel died on March 30, 1873, while returning from a trip to Le Havre innorthwestern France, where he had spoken of Joan of Arc and her hallucinations(Constant-Trocmé 1970; Semelaigne 1930).

Figure 4. Bénédict-Augustin Morel (1809–1873) (OW collection).

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On June 26, 1911, the French Medical-Psychological Society awarded the philosopherGeorges Genil-Perrin (1882–1964) the Prix Semelaigne for a dissertation that wouldbecome his doctoral thesis in medicine in 1913: Histoire des origines de l’évolution del’idée de dégénérescence en médecine mentale (History of the origins of the idea ofdegeneration in the medicine of mental illness; Genil-Perrin 1913). The jury was presidedover by Gilbert Ballet (1853–1916). At the beginning of his thesis, Genil-Perrin explained,“The idea of mental degeneration is a poorly defined notion.” For him, this idea was“based on elements borrowed from heredity and the problem of physical and moralrelationships” and results from positivism, which makes “psychology into a chapter ofbiology.” Thereby freed of metaphysics, it became “a vast anthropological-psychiatricconcept” (Jennekens 2014). However, Morel’s initial approach was entirely different.What influenced him?

Johannes Burchart, in his thesis presided over by Stahl in 1706 (Burchart 1706),developed the idea of a heredity of predisposition, which became the dissimilar heredityof Philippe Pinel (1745–1826). In his 1801 Traité médico-philosophique sur l’aliénationmentale (Medical-philosophical treatise on mental illness), Pinel saw this form of heredityas the origin of madness, an idea that François-Emmanuel Fodéré (1764–1835) carriedforward in 1832, followed by Jean-Étienne Esquirol (1772–1840) in 1838. The primitiveerror of this theory was to mix exact observations with false interpretations, confusing therole played by the transmission of a trait with the influence of social milieus andupbringing in the development of behaviors considered pathological. Nonetheless, it wasa theory Morel embraced.

The concept of degeneration developed by Morel was intrinsically linked to hisCatholicism, to the doctrine of original sin, and to Adam’s error, which were believedto have caused humanity’s fall. Morel participated in the discussions of a cenacle that alsoincluded Laurent Cerise (1807–1869) and Philippe Buchez (1796–1865). Their goal was topromote social medicine, an extension of their shared Catholic faith (Carbonel 2010).Since the Bible and Genesis were at the root of their thinking, Morel, a monogenist anda fixist, conceived of mental pathology as “an unhealthy deviation of a primitive type”(Morel 1857, 2) in which the latter was free of any defects. Deviation occurred, however,because of “the original degradation of human nature,” or the price paid for sin. Theparadox of Morel’s thinking, which aimed to be scientific but remained theistic andpolitical, was that it presented degeneration as a biological danger, harming social orga-nization through the hereditary accumulation of transmitted defects, which ultimately andinexorably sterilized the human race. The medicine of mental illness, however, worked “forregeneration and calls on the assistance of all those entrusted with the well-being and thefate of the population, all those who have the means to carry out the improvements thatmedical science submits to them” (Morel 1857, 6; see Figure 5). Regeneration was seen asthe task of public health, based on conservative “moral law,” in which the preceptsdictated by Catholicism took precedent—namely, “the natural order of the creator,”centered on traditional family values, “domestic virtues,” and authority. Morel’s reactionto the revolutionary events of 1848 is evident, whereas initially he did actually seek toimprove the conditions of workers and the poor.

Influenced by the “zoological philosophy” of Jean-Baptiste deMonet de Lamarck (1744–1829)published in 1809, and Histoire générale et particulière des anomalies de l’organization chezl’homme et les animaux (General and specific history of anomalies in the organization of men

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Figure 5. Cover of B.-A. Morel’s most famous work in 1857 (OW collection).

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and animals) published in 1832 by Étienne Geoffroy Saint-Hilaire (1772–1844), Morel saw“habits” as the driver of the transformations that were passed on. Unhealthy deviations resultedfrom the pathogenic conditions of one’s milieu and from repeated automatisms, leading tomorphological as well as psychological adaptations. These adaptations were passed on fromgeneration to generation, always toward progressive decadence. Disharmony in the body anddysfunction of the nervous system, both hereditarily and progressively transmissible, defined theinexorable fall—that is, degeneration. To illustrate his ideas, Morel added an atlas of engravings tohis text, showingmicrocephaly and various cranial deformations (Figure 6). Alongside anatomicaltraits, Morel introduced a new etiological classification of mental illness, which was based onintoxication (alcohol, dietary deficiencies), social milieu (unhealthfulness, poverty, industry),“moral malignity,” acquired (pellagra, scrofula) or inherited (epilepsy) morbid conditions, andso forth.

In sum, two laws governed degeneration: “the law of double fertilisation in termsof physical malignity and moral malignity, and the law of progressivity ofdegeneration”(Morel 1857, 78). These became “Morel’s laws” for his champions. Forexample, an alcoholic’s son carries the physical defect of the addicted parent and themoral defect of his dissolute life, making him an irremediable degenerate, capable only ofproducing even more degenerate offspring. Using the term “heredity of transformation,”Morel generalized the inevitability of disease transmission. In this way, the first genera-tion, in which “a nervous temperament” predominates, saw various neuroses (e.g., epi-lepsy and hysteria) and cerebral hemorrhages multiply in the next generation. Morelinsisted repeatedly on a factor in addition to those mentioned above: the influence ofplaces and climates in the emergence of degeneration. Swamps, cold climates, andhumidity were presented as the most harmful, causing fevers and transmissible defects.

Finally, Morel also included predispositions specific to race, the hierarchy of which wasunquestionable for him. This position was ambivalent in that he recommended “racialcrossbreeding” to regenerate humanity, influenced as he was by animal rearing andhorticulture. Is it enough to “proclaim the need for racial crossbreeding so that humanity’sinterests are protected in the future? These interests would, on the contrary, be singularlycompromised if moral culture failed to fertilize the vigorous products resulting fromcrossbreeding and marriage between different social classes” (Morel 1857, 75).

In 1895, Valentin Magnan (1835–1916) and Paul-Maurice Legrain (1860–1939) summedup the concept of degeneration, at a time when nearly all alienists subscribed to it:

Degeneration is the pathological state of the individual that, compared to his most immediateprogenitors, is constitutionally less resistant psychophysically and can only partially achievethe biological conditions of the hereditary fight for life. This weakened resistance results inpermanent stigmata that are essentially progressive, without intercurrent regeneration, lack-ing which the species is more or less rapidly annihilated. (Magnan and Legrain 1895, 79)

This concept included social, biological, and psychological data in a single category, providinga facile explanation, lacking any real scientific basis, as to the complex question of the origin ofmental disorders. To this day, the etiological question has not been fully resolved.

In particular, Charcot focused on hereditary predisposition as well as dissimilar heredity. Forexample, a young woman who suffered from hysteria in adolescence and from delirious ideasandmania in adulthood, eventually dying in a state of dementia. Amorbid predisposition led tothe successive exteriorization of “pathologies of the same kind, manifesting the same

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pathological aptitude of the degenerate race by various disturbances,” according to Morel. Hisdoctrine, as Charcot understood it, took the form of a vast etiological concept situated at thefoundation of all psychiatric and neurological diseases of the nervous system.

Figure 6. Plate IX of B.-A. Morel’s atlas: Degeneration of the shape of the skull (OW collection).

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Influence of Jacques Joseph Moreau de Tours

After AlfredVelpeau (1795–1867) andArmandTrousseau (1801–1867), Jacques JosephMoreaude Tours (1804–1884; Figure 7)—who was the third disciple of Pierre Bretonneau(1778–1862)—a famous physician from the western French city of Tours. A resident underJean-Étienne Esquirol (1772–1840) for four years at the Charenton asylum, he adopteda scientific approach in his thesis (Moreau 1830) and pursued it throughout his career. He sawthe brain, the organ of thought, as being subject to functional disorders, whether they werelesional or not, which led him to consider madness as an organic disease. Heredity, he believed,was the etiology: “Via the path of heredity, and by this path alone, we can work our way back tothe psycho-organic source of these phenomena, penetrating and reading, so to speak, theintimate texture of the organ governing their external manifestation” (Moreau de Tours 1859).He disagreedwith those for whomheredity only be applied to intellectual phenomena: “Heredityexpresslymeans the seminal transmission, not ofmoral qualities of one individual to another, butrather nervous or vital forces.” The organization of sensory organs, indispensable for psychicfunctioning, was transmitted via heredity, as was their own functioning: “Almost equal tosensations, affective passions depend on the organisation; they share its vicissitudes. Like it,they must be transmitted by heredity” (Moreau de Tours 1859, 13). A hereditary predispositionexisted; life events would trigger mental pathology. The influence of the environment becamecrucial as to whether or not insanity emerged. He admitted he could not establish the intimatenature whereby mental states were transmitted, but he held that symptoms may differ betweendifferent individuals of the same family: One had tics, the other stuttered, and the third waseccentric and eventually went insane. This notion of predisposition and its corollaries wereadopted by Charcot, notably to explain the genesis of hysteria. Climate, morals, nutrition, andmany other circumstances might all be causes of deviation from the standard of normality.

Validation by Jules Dejerine

In his 1886 agrégation thesis, entitled Hérédité dans les maladies du système nerveux, JulesDejerine (1849–1917) stated:

Figure 7. Jacques-Joseph Moreau de Tours (1804–1884) (© BIU santé, Paris).

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Morel, Lucas, and Moreau de Tours, physicians from our country, were the initiators of thisapproach. Especially Morel, who formulated and resolved the question for mental illnesses, inseveral admirable works. He showed how these conditions were interlinked and also linked tothe major neuroses by the laws of heredity and degeneration, and inaugurated a fecund researchmethod, carried forward by all contemporary alienists.…What Morel did for mental illnesses iswhat clinical medicine is currently doing for the other nervous system diseases. This is the typeof research that Mr Charcot has repeatedly stressed in his lessons for several years. (28)

Heredity and the concept of degeneration in Charcot’s work

Before 1882: Expression of the histopathological description

Whereas Charcot merely tried to find correlations between his clinical observations and hisanatomical findings at the beginning of his career, the creation of the Chair of the Clinic ofNervous System Diseases in 1882 can be seen as the moment when, in order to teach hisstudents about the diseases he helped identify, he had to research and conceive of an etiology foreach one. At the beginning of his career, mostly focused on geriatrics, the predominantexplanations were climatic and environmental factors, such as cold temperatures, humidity,and diet. His thesis on chronic rheumatism (polyarthritis, degenerative arthritis) and gout wasan example of this.

In the first description of Parkinson’s disease in 1861 by Charcot and Alfred Vulpian(1826–1887), degeneration was not mentioned. Rather, emotions were presented as play-ing a preponderant triggering role, in addition to “the combination of cold temperaturesand humidity” (Charcot and Vulpian 1861).

In their Clinical Lectures on the Diseases of Old Age (originally published in 1874), theterm “degeneration” was only used to qualify the excess fat on cardiac muscle observed incertain gout patients (Charcot and Ball 1874). Similarly, in the first release of ClinicalLectures on the Diseases of the Nervous System (originally published in 1872), the word“degeneration” did not appear in the body of the text, and only three times in thefootnotes, to describe the changes in appearance of anatomopathological cross-sectionsof muscular fibers (Charcot and Bourneville 1872).

Charcot’s initial uses of the term “degeneration” are only a description of visuallyobservable transformations of tissues examined under the microscope, as caused bypathology. This word did not refer to the etiology of the pathological process. His usagewas thus aligned with the definition of the lexicographer Émile Littré (1801–1881) in 1873:“Damage that leads to the transformation of an organ’s tissue into an essentially morbidmaterial” (Littré and Robin 1873).

The descriptions of anatomopathological lesions observed by Charcot and Vulpian incases of locomotor ataxia in 1862 (Charcot and Vulpian 1862) did not employ the word“degeneration” at all. However, in the first description of multiple sclerosis, it is used todistinguish lesions viewed under the microscope:

Sclerosis of the spinal cord, in the strictest sense, must be carefully distinguished from thegranular degeneration followed by atrophy that frequently occurs in the same organ due tocertain conditions of the brain or the spinal cord itself. This degeneration is sometimes found,over significant lengths, in the anterolateral tracts or the posterior tracts, either on one side,or symmetrically, on both sides at once.” (Charcot 1865, 472)

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After 1882, heredity became a predominant etiological entity in neurology

For Goetz, Bonduelle, and Gelfand the turning point came after the 1881 World Congressof Medicine in London. Supporting his findings with statistics, Wilhelm Erb (1840–1921)demonstrated that more than 90% of cases of locomotor ataxia (tabes dorsalis) were linkedto syphilis, as also argued by Alfred Fournier (1832–1914; see Goetz, Bonduelle, andGelfand 1995) in France. During this congress, Pasteur’s theory on the microbial origin ofinfections was widely hailed. However, a number of physicians did not accept this theory.Not the least of them was Charcot, who clearly stated his objections during his report onthe Prix Civrieux awarded by the French Academy of Medicine in 1883 to his studentsLouis Landouzy (1845–1917) and Ballet, who had examined “research into the causes oflocomotor ataxia.” Charcot saw this work as confirming his personal conviction:

For them, the true, essential, and determinant cause of tabes, the cause that dominates,commands, and absorbs all others, and the cause in the absence of which, perhaps, the othersare powerless, is hereditary nervous predisposition.… Tabes is one of the clinical aspects that,when examined in depth, reveals the nervous defect that the patients inherited from theirprogenitors. … This view is obviously not new, but it is necessary to highlight it once again,to establish the absolute and rigorous reality based a sufficient number of observations,studied with a high level of clinical expertise and patiently examined from the etiologicalperspective. (Charcot 1883, 1451)

Here is how Henry Lamy (1864–1909) explained Charcot’s reasoning:

In light of impressive statistics, there is now a tendency to view certain cerebrospinal diseasesas being produced by syphilis, whereas the related anatomical lesions do not at any timepresent the characteristics generally associated with syphilitic lesions. Whatever the merits ofthis way of thinking, it is not aligned with the scientific method that has guided medicine inour century to its greatest discoveries. It goes without saying that what we know of thedamage caused by syphilis in the organs remains quite rudimentary; it may be that, likecertain poisons, it acts electively in the nervous centers, on a given differentiated system,initially affecting only the essential element; but this remains only a curious hypothesis, andnot a lodestar in the study of how syphilis affects the nervous system. Until the results ofbacteriological research have achieved the accuracy that is required today for the study ofinfectious diseases, only pathological anatomy and clinical medicine can determine, insofar aspossible, the relation between syphilis and nervous diseases.” (Lamy 1893, 5)

Charcot would remain convinced until his death that syphilis was only one revealing agentamong others, acting through hereditary predispositions. For example, in his TuesdayLesson on January 10, 1888, he noted: “In all ataxics, I believe there to be somethinghereditary, but this is especially true in early ataxics.”

On Tuesday, March 13, 1888, Charcot generalized heredity as etiology to all diseases ofthe nervous system:

On one hand, Friedreich’s ataxia is hardly common ataxia and on the other, there is morethan ever good reason to believe that common ataxia is a hereditary disease, in the same waythat other members of the neuropathological family are. In addition, Friedreich’s ataxia is not,in the strictest sense of the word, a hereditary disease so much as a family disease,a generational disease, which is not quite the same thing. … As I mentioned earlier, theetiological characteristics of Friedreich’s ataxia are remarkable, leading some authors to call ithereditary ataxia. But, as I have just told you, real ataxia is also a hereditary disease. Thisbears repeating, even though I have already mentioned it to you several times. In such cases,

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it is not, of course, a matter of homologous heredity, which is very rare, but rather theheredity of transformation, which, as you know, is the rule. (258)

He was speaking of Morel’s heredity of transformation, Pinel’s dissimilar heredity, andLucas’s heredity of metamorphosis (see Table 1).

Bearing witness to the “extemporaneous” nature of his consultations, his TuesdayLessons, all of which were transcribed for 1887–1889, reveal that Charcot focused inparticular on his patients’ family histories. These were significant in his view, and hebelieved they frequently provided him with the origin of the disease in question: “Theclinician only has an episode to work with, if he wants to limit himself to studying thepatient himself, and not take the entire family history into account” (Charcot 1887). Hereare a few examples:On Tuesday, 17 July 1888, Charcot lectured on chronic Huntington’s disease:

Thus Huntington’s chorea is like many other nervous system and muscular conditions newlyintroduced in the nosography, for example: Thomsen disease, Friedreich’s ataxia, andpseudo-hypertrophic paralysis described for the first time by Duchenne de Boulogne [seeFigure 8]. All these conditions, as you know, are both similar hereditary diseases and familydiseases, while manifesting the heredity of transformation in various ways.

These diseases were thus accurately identified as hereditary, but confusion still surroundedtheir transmission (Figure 9):

Similar heredity appears to be one of the major etiological characteristics of the disease, whichdevelops inevitably and is perpetuated from generation to generation, most often in the absenceof an identifiable occasional cause. Without apparent reason, it one day emerges and develops,at exactly the most opportune moment, nearly always at around the same age. (Charcot 1887)

Charcot established a parallel with Sydenham’s chorea, for which he frequently observed“hereditary of transformation.” The existence of a case of epilepsy or hysteria in the familyconfirmed his idea of heredity of transformation: “It is truly a basic observation in thechoreic patient, and you know this is an aetiological fact I often have the occasion to pointout in the patients who come for the Tuesday consultation.” Charcot’s refusal to accept thesyphilitic origin of tabes was analogous to his view that chorea and acute rheumatoid

Figure 8. Tree drawn by Charcot during his lesson on Tuesday, July 17, 1888 (OW collection).

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arthritis of the joints occurred together simply due to a frequent coincidence, “a certainaffinity,” but “not at all because they [were] identical and of the same nature.”

Charcot cited shaking as another example of similar heredity:

This trembling may present, in certain subjects, sporadically; that is, without precedents orconcomitants in ascendants or collaterals; but in other instances, it is indeed similar toHuntington’s cases; that is, a family disease, strictly speaking. Most often, shaking occurs inchildhood and is passed down by similar hereditary. (Charcot 1887, 544; see Table 1)

On Tuesday, February 21, 1888, Charcot questioned a 21-year-old man suffering from tics:“What is more, you know that having tics in a family is not without significance. Tics area special mark.” What followed was a thorough interrogation on personal and familyantecedents. The patient, it turned out, also had a folie du doute characterized by the fearof rabies at the sight of an animal. He had two brothers and a sister with tics: “When thereis one ticcer in a family, it is rarely an isolated case.” In one 1886 lesson that was notpublished until 1893, Charcot discussed laryngeal noises, presented as hysterical anddistinct from Gilles de la Tourette disease:

Mr. Gilles de la Tourette ingeniously grouped together sudden involuntary, automaticutterances that are often vulgar or obscene, but are said aloud and intelligibly, under thename of coprolalia. This often affects well-educated people with proper upbringing. … Take,for example, the case reported by Professor Pitres, of a young lady from Bordeaux, aged

Figure 9. Page 145 of Volume 2 of the consultations du Mardi, 1889 (OW collection).

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fifteen, with an insane aunt and a ticcer father. She herself was a ticcer who, during her fits,uttered the most filthy language. (Charcot 1893)

In response to a case of peripheral facial palsy, Charcot noted, “we now know this is nota condition where cold temperatures are the cause, but rather a true nervous disease.” For him,the families of these patients revealed cases of “nervous phenomena of another kind, insanity,locomotor ataxia, and so forth.” That is, they revealed heredity of transformation. Charcotmade a side note to the effect that Jews would be particularly prone to familial facial palsies.

Once again, Charcot’s thinking was the same for Graves’ disease; he stated it “is oftena family disease, passed on by heredity and involving insanity, epilepsy, and so forth. It isin the same category and it also has common links with the arthritic family for the entireseries.” In addition: “Alcoholics are not always what they are superficially assumed to be.Alcoholism is sometimes a kind of constitutional vice, a hereditary defect.”

On Tuesday, December 6, 1887, Charcot explained how he saw heredity of transforma-tion: “Nervous diseases are almost never passed on in the same form. You must thus notreason that locomotor ataxia engenders locomotor ataxia, and general paralysis generalparalysis. This is not at all true. Heredity proceeds by transformations. A paralyticengenders a hysteric and a hysteric a paralytic.” On Tuesday, July 10, 1888, he summarizedthe laws of heredity this way:

Take what I proposed to call the neuropathic family. I use this term to distinguish all conditions ofthe central nervous system and neuromuscular system that are organic or, on the contrary,without any appreciable anatomic lesions, and that are linked by heredity. You are well aware thathere we have to distinguish, together with homologous heredity, dissimilar heredity or heredity oftransformation, which may be seen much more frequently than the former. (Charcot 1893, 455)

A genetic tree created for the examination of “typical spinal infantile paralysis,” undoubt-edly a case of poliomyelitis, showed the range of antecedents, which, to a current-dayobserver, seem in no way hereditary: epilepsy, phobia, melancholy, tuberculosis, gout(Charcot 1889). A variety of pathologies were thus tied together, leading to a vagueconcept of dissimilar heredity and thus to a scientific impasse, but one that opened theway to ideological deviations (Pinell 2001).

After 1882, Charcot no longer wrote any articles himself, except in English. He left thetask of publishing research results from La Salpêtrière to his students. It is thus interestingto analyze the work of two of his most faithful, prolific, and zealous champions, CharlesFéré (1852–1907) and Georges Gilles de la Tourette (1857–1904), both of whom demon-strated unfailing and fervent veneration of Charcot.

Charles Féré and the neuropathic family

Charles Féré was Charcot’s resident in 1881 and defended his thesis before a jury presidedover by Charcot on March 18, 1882. The theme of heredity can be found throughout hiswork and he constantly focused on fighting all forms of degeneration. Féré, like Charcot,did not research the origins of heredity but limited himself to observing the transmissionof nervous diseases down through the generations, whatever the biological processes; thatis, he was satisfied with the genealogy of the clinical history alone (Gelfand 1987). Hechampioned eugenics, the only way he believed humanity could be saved (Courtin 2007).After an article in Les Archives de Neurologie (Féré 1884), his emblematic book was

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published in 1884, then reissued and completed in 1894: La famille névroprathique, théorietératologique de l’hérédité, de la prédisposition morbide et de la dégénérescence (Theneuropathic family, a teratological theory of heredity, morbid predisposition, and degen-eration; Féré 1894). Féré coined the term “famille névropathique” with which Charcotagreed and used from then on. For Féré, because Lucas, Morel, and Moreau de Tours wereonly interested in mental disturbances, they “only considered other nervous diseasessecondarily and in general.” Taking an approach opposite to Morel’s, Féré made nometaphysical references and adhered to Darwin’s theory of a fight for life that led toselection. He defended the transmissibility of acquired traits, citing hysteria as an example:“Concerning hereditary influence, there is no nervous condition in which it is more clearlymanifest than in hysteria.” For Féré, hysteria arose from direct heredity and dissimilarheredity. All pathologies of the nervous system may be associated with hysteria, the“sufficient predisposition,” and the stigmata identified by Charcot externalized thispredisposition.

From mental diseases, Féré extended the study of heredity and degeneration to neuro-logical and neuromuscular diseases: for example, tics, functional spasms (neuropathictorticollis, writer’s cramp, i.e., dystonia), shaking, migraine, epilepsy and neurasthenia,and Friedreich’s ataxia. He adopted a view of locomotor ataxia that was identical toCharcot’s. As for amyotrophic lateral sclerosis and multiple sclerosis, he doubted theywere hereditary. The final chapters of the 1894 version of his book covered “the terato-logical stigmata of degeneration.” The “objective signs of degeneration” were as significantas heredity, and the moral and physical causes had the same implication. He alsoexplained: “The traits that are the stigmata of degeneration have characteristics that donot belong to the race and that, passed down in the family in which they have appeared,tend to function in the same way as an accident and remove the family from the race”(317). As examples, he cited variations in skull size and shape, various unusual hairimplantations, ear lobe deformations, dental implantation disorders, pectus excavatum,lumbar pilosity, and so forth. It may be relevant here that after the defeat in the 1870Franco-Prussian War, people in France were haunted by the fear that the decadence of the“French race” would make it impossible to take revenge. Degeneration and decadencewere part of the same ideology. Féré did not refer to any of the work by his contemporarybotanists, naturalists, or biologists, even though they could have pruned back his theory ofdisease transmission. During his Tuesday Lessons, Charcot cited Féré’s book multipletimes, always with effusive praise, until it was no longer clear who was the teacher andwho was the student.

Féré and Charcot shared the same thinking on heredity—that is, a familial predisposi-tion to disease. In this situation, a family carried a susceptibility to neurological disordersthat might or might not develop, depending on the environment. If the family member leda quiet and healthy life, he or she could potentially avoid neurological manifestations evenwhen carrying the propensity for disability. On the other hand, the same predispositionwould unleash severe disease if the patient’s lifestyle or environment was unhealthy. Thistopic of “agents provocateurs” (triggering factors) was discussed by Charcot in hisNovember 15, 1887, Tuesday Lesson, during which he stressed the role of trauma(Charcot 1887).

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Dejerine wrote in 1886, “Féré deserves credit for being the first to study the questionwith an overarching approach. His Famille névropathique is the most important workpublished in this field since Morel” (Dejerine 1886).

In 1888, Féré published Dégénérescence et criminalité, essai physiologique (Féré 1888) asa follow-up, and in line with the recent books of César Lombroso. The chapters oncriminal heredity and anatomical and physiological traits in criminals returned over andover to all the clichés of the time, conditioning both thought and society in ways thatwould engender the worst aberrations of the twentieth century.

It must be noted that immediately after his stay at La Salpêtrière (1885–1886), SigmundFreud (1856–1939) adopted the doctrine of the neuropathic family but, when he devel-oped his own theory of hysteria’s origins, he questioned its validity:

It will undoubtedly soon be necessary to review and correct the etiological theories defendedby Charcot in his doctrine of the neuropathic family and on which he founded his globalunderstanding of nervous diseases. Charcot so overestimated the etiological role of hereditythat no place remained for other neuropathic etiologies. (Freud 1893, 162)

Georges Gilles de la Tourette and hysteria

For Georges Gilles de la Tourette, his Traité clinique et thérapeutique de l’hystérie d’aprèsl’enseignement de La Salpêtrière (Clinical and therapeutic treatise on hysteria based on theteachings at La Salpêtrière), published in three volumes from 1891 to 1895, was his mostimportant work. Although it did not garner lasting fame, it faithfully reflected allCharcot’s lessons and thinking on this pathology: “Mr. Charcot taught that the primordialcause of hysteria was heredity, whether it was similar: hysterical mother, hystericaldaughter; or whether it entailed transformation: the progenitor(s) or their descendantssuffered from a nervous condition other than hysteria itself. Beside heredity, there are onlyagents that trigger neurosis” (Gilles de la Tourette 1891–1895, 68).

“The continuity of germinative plasma,” according to August Weismann (1834–1914),explained the inexorability of the transmission of acquired defects and disorders, the ultimateresult of which could be none other than degeneration. To list the triggering agents of hysteria,Gilles de la Tourette used elements from the thesis of Georges Guinon (1859–1932), hissuccessor as Charcot’s resident (Guinon 1889). First among these agents were “violent moralemotions,” whose role in the development of hysteria “had always been acknowledged, andtheir importance became even greater when the mental state of hysterics, characterised bysuggestibility, was recognised.” Gilles de la Tourette went on to list the following influences,with relevant observations and discussion: trauma; acute and chronic infectious diseases(tuberculosis); diseases of the genitalia; lead poisoning or addiction to alcohol, tobacco, ormorphine; and all nervous diseases (tabes, epilepsy, tic disorder, myopathy).

Gilles de la Tourette reminded his readers that Hippocrates already saw hysteria asa hereditary pathology. To confirm this, he returned to the statistics of Pierre Briquet(1796–1881; Briquet 1859) and those of a Swiss student of Charcot, Émile Batault(1859–1929), whom he himself oversaw during his time as senior resident (Batault1885). This explains the “law of preponderance in the transmission of traits” whereby“it is not always the healthy individual who predominates, on the contrary; in the largemajority of morbid cases, transmission occurs in childhood, even though only one of histwo progenitors is sick” (Gilles de la Tourette 1891–1895, 43).

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Paul Peugniez (1859–1943), in his thesis before a jury presided over by Charcot onJuly 24, 1885, stressed the following: “First and foremost, it is the disastrous law of nervousheredity that causes the development of hysteria in youngsters.” He did not fail tounderscore such decisive causes as “abuse, frightening experiences, moral emotions, andceremonies.” Many of these children suffered from what is currently known as attentiondeficit hyperactivity disorder. Others had authentic epilepsy, or migraine, whereas stillothers had nascent psychosis.

On November 28, 1888, Grégoire Breitman (1859–1914), a physician from the city ofAnanyiv in Moldavia, defended the first thesis on Gilles de la Tourette syndrome since theseminal article’s publication in 1885, with Charcot presiding over his jury: “Alienists suchas Magnan and his students, Legrain and Saury, see in echolalia, coprolalia, and echokin-esis an episodic syndrome of la folie des dégénérés” (Breitman 1888). Paul-MauriceLegrain (1860–1939) and Honoré Saury (1854–1906), disciples of Valentin Magnan (-1835–1916), introduced the concept of bouffée délirante (brief psychotic disorder) into thepsychiatric nosology; this was after both had done work on la folie des dégénérés (insanityof degenerates), with Legrain writing his thesis on the subject and Saury a book.

Breitman, a student alienist at the Vaucluse asylum near Paris, wanted to study theheredity of involuntary imitation symptoms in order to clarify the role of “degeneration”in their genesis, given that:

As the semiology of hereditary degenerates grows more detailed, exact, and manifest, we arerelegating the search for the original flaw in the various forms of alienation to a secondaryposition,” because “the aim is to find out whether, by studying the semiology of each psychicstate and by grouping the signs into syndromes, we can, by deduction, demonstrate themanifestly degenerative hereditary origin. (7)

He explained that “under the combined influence of peripheral and central excitations, wewill see degenerates, these future candidates for mental alienation, executing a series ofbizarre actions, designated as ‘Latah, Jumping, and Myriachit’ by foreign authors.”Breitman showed, based on several observations he had collected, that echolalia, copro-lalia, and echokinesis could be seen in various types of mental alienation, especially indeliriums, and concluded that “echolalia, coprolalia, and echokinesis accompanied by ticscan make up a perfectly independent morbid syndrome with a determined progression,the tic disease or Gilles de la Tourette disease. Patients with this disease are degenerate”(Walusinski 2019).

From yesterday to today

With his usual prudence, Charcot first had his students publish his ideas on the hereditaryetiology of nervous system diseases before turning them into a doctrine he himselfprofessed, as one can read in the Tuesday Lessons from 1887 onward, when he beganto treat patients from the external consultations department. He used genealogical trees tosupport his demonstration. The belief in transmission of acquired traits was widespread atthe time and provided a rather simple response to difficult questions. Degeneration,elevated to the rank of hereditary defect, not only applied to nervous system damagebut played a role in explaining individual behaviors, and beyond that social behaviors, asin the books of Emile Zola.

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One of the remarkable elements of Charcot’s hereditary thinking was the concept ofheterogeneous expressions of disease: Various members of the same family could havediseases of the nervous system but different diagnoses—epilepsy, melancholia, infantile spinalparalysis, and so on. At first glance, this type of analysis might be dismissed by modernneurologists as naive, but conceptually, such approaches involving multiple phenotypes withone genotype are highly pertinent today. In 2013, Lesage and colleages identified disease-causing repeat C9orf72 gene expansions in a subset of patients from a large cohort withdifferent forms of Parkinsonism, extending the clinical phenotype associated with theseexpansions from degenerative dementias—including Alzheimer’s disease and amyotrophiclateral sclerosis—to Parkinsonism (Lesage et al. 2013). Charcot summarized his thought ina limpid manner by this quote: “Le malade n’est qu’un épisode, l’ennemi c’est la famille” (thepatient is only one episode; the enemy is the family), which provides the key to Charcot’s viewof all neurological diseases. It also links all areas of pathogenesis—hereditary, toxic, andinfectious—allowing nonhereditary triggering factors to play a role in disease manifestationwhile remaining secondary issues relative to hereditary factors (Charcot 1887).

The swing of the pendulum in scientific discoveries had set genetics in the foreground ofetiological research on nervous system diseases but did not validate the vague concepts usedby Charcot. Like a nod to the past described above, the discovery of bits of the viral genome insome of our chromosomes could become a potential explanation for so-called prion diseases,illustrating the old meaning of “degenerate”: “To lose the qualities of the lineage.” Themeaning of degeneration as conceived by Morel is no longer current, but the expression“neurodegenerative diseases” is frequently used today, referring to structural and metabolicmodifications to cells in the nervous system. Charcot obviously could not have suspected thesephenomena of disintegration, potentially programmed in the genome. A neuropathologistwho studied under Pierre Marie, Ivan Bertrand (1893–1965), entitled one of his works Lesprocessus de désintégration nerveuse (Processes of nervous disintegration) in 1923; he probablybetter expressed the processes under way in these pathologies than if he had employed theword “degeneration,” too often used with different meanings (Jennekens 2014).

As Charcot possessed none of Pasteur’s works in his library and made no explicitallusion to microbial theory, he did not realize Pasteur’s importance, unlike some of hisstudents, such as Victor Cornil (1837–1908) and Pierre Marie (1853–1940), or his alterego, Alfred Vulpian (1826–1887).

Why did Charcot so dogmatically believe in hereditary causes, when he was so demandingof experimentally documented data in the rest of his anatomoclinical work? Without posingany real questions, he embraced hereditary etiological explanations where elsewhere he arguedagainst blind acceptance of prior theories or biases, always charting his own path. Severalhypotheses are possible: heredity as a seemingly scientific and simple explanation, one that allphysicians can test on a daily basis by observing their patients and their patients’ families. Butlike all dogmas, this type of explanation rests on a belief whose apparent validity is based solelyon its longevity, dating back to antiquity (Horrobin 1976); the underestimation of Pasteur’sdiscoveries (Gaudillière and Löwy 2014); the adherence to Darwinian concepts, perhaps withthe prescience of the future discovery of their biological basis; and the influence of theintellectual milieu in Paris at that time, which focused attention on a young science, anthro-pology, still marked by racism and the fear of losing the supposed superiority of whites overblacks, and of French people over Germans, given the “vengeful spirit” at the end of thecentury (Poirier 1983).

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Charcot often overlooked the socioeconomic conditions of his patients, focusinginstead on familial heredity, which was a way to avoid making outright social or politicalstatements about the causes of disease. Through his adherence to a progressive andanticlerical ideology, Charcot opposed the powerful religious beliefs that existed in hissociety. Heredity depended on biological laws, yet to be discovered, but they did not needthe divine to explain disease (Brais 1993; Lalouette 2002). David Horrobin (1939–2003)has summarized these perspectives on disease inheritance as follows: “The history ofscience has repeatedly shown that when hypotheses are proposed, it is impossible topredict which will turn out to be revolutionary and which ridiculous. The only safeapproach is to let all see the light and to let all be discussed, experimented upon,vindicated or destroyed” (Horrobin 1976).

Acknowledgments

Many thanks to Jacques Poirier, Hubert Déchy, and the reviewers for their attentive readings andsuggestions, and to Anna Fitzgerald for her translation.

Disclosure statement

No potential conflict of interest was reported by the author.

Funding

The author received no financial support for the research, authorship, and/or publication of thisarticle.

ORCID

Olivier Walusinski http://orcid.org/0000-0001-6927-7946

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